Nephrology Flashcards
(104 cards)
1
Q
Answer these four questions when solving acid-base problems:
A
- What is the primary disturbance?
- Is compensation appropriate?
- What is the anion gap?
- Does the change in the anion gap equal the change in the serum bicarbonate concentration (a value called the delta-delta)?
2
Q
Acidemia
A
pH <7.38
3
Q
Metabolic acidosis
A
= [HCO3] <24 meq/L
4
Q
Respiratory acidosis
A
Respiratory acidosis = arterial PCO2 >40 mm Hg.
5
Q
Alkalemia
A
pH >7.42
6
Q
Metabolic alkalosis
A
Metabolic alkalosis = [HCO3] >24 meq/L
7
Q
Respiratory alkalosis
A
Respiratory alkalosis = arterial PCO2 <40 mm Hg.
8
Q
Metabolic Acidosis Expected Compensation (Acute)
A
Acute: Δ arterial PCO2 = (1.5)[HCO3–] + 8 ± 2
Failure of the arterial PCO2 to decrease to expected value = complicating respiratory acidosis
Excessive decrease of the arterial PCO2 = complicating respiratory alkalosis
9
Q
Metabolic Acidosis Expected Compensation (Chronic)
A
Chronic: Δ arterial PCO2 = [HCO3–] + 15
Failure of the arterial PCO2 to decrease to expected value = complicating respiratory acidosis
Excessive decrease of the arterial PCO2 = complicating respiratory alkalosis
10
Q
Respiratory acidosis Expected Compensation (Acute)
A
cute: 1 meq/L ↑ in [HCO3–] for each 10 mm Hg ↑ in arterial PCO2
Failure of the [HCO3–] to increase to the expected value = complicating metabolic acidosis
Excessive increase in [HCO3–] = complicating metabolic alkalosis
11
Q
Respiratory acidosis Expected Compensation (Chronic)
A
Chronic: 3.5 meq/L ↑ in [HCO3–] for each 10 mm Hg ↑ in arterial PCO2
Failure of the [HCO3–] to increase to the expected value = complicating metabolic acidosis
Excessive increase in [HCO3–] = complicating metabolic alkalosis
12
Q
Metabolic alkalosis Expected Compensation (Acute)
A
0.7 meq/L ↑ in arterial [HCO3–] for each 1 mm Hg ↑ in PCO2
This response is limited by hypoxemia
13
Q
Respiratory alkalosis Expected Compensation (Acute)
A
Acute: 2 meq/L ↓ in [HCO3–] for each 10 mm Hg ↓ in arterial PCO2
Failure of the [HCO3–] to decrease to the expected value = complicating metabolic alkalosis
Excessive decrease in [HCO3–] = complicating metabolic acidosis
14
Q
Respiratory alkalosis Expected Compensation (Chronic)
A
Chronic: 4 meq/L ↓ in [HCO3–] for each 10 mm Hg ↓ in arterial PCO2
Failure of the [HCO3–] to decrease to the expected value = complicating metabolic alkalosis
Excessive decrease in [HCO3–] = complicating metabolic acidosis
15
Q
Anion Gap
A
anion gap = [Na+] − ([Cl–] + [HCO3–]).
Normal anion gap is 12 ± 2 meq/L
16
Q
When the primary disturbance is not a metabolic acidosis, the anion gap helps detect
A
“hidden” anion gap metabolic acidosis.
17
Q
An anion gap (<4 meq/L) suggests
A
multiple myeloma or hypoalbuminemia
18
Q
Common causes of anion gap acidosis include:
A
- DKA
- CKD
l3. actic acidosis (usually due to tissue hypoperfusion) - aspirin toxicity
- alcoholic ketosis
- methanol and ethylene glycol poisoning
19
Q
Common causes of normal anion gap metabolic acidosis include:
A
!. GI HCO3– loss (diarrhea)
- kidney HCO3– loss (ileal bladder, proximal renal tubular acidosis)
- reduced kidney H+ secretion (distal renal tubular acidosis, type IV renal tubular acidosis)
- Fanconi syndrome (phosphaturia, glucosuria, uricosuria, aminoaciduria)
- carbonic anhydrase inhibitor use
20
Q
Urine Anion Gap
A
defined as (urine [Na+] + urine [K+]) – urine [Cl–].
UAG is normally between 30 to 50 meq/L
21
Q
Negative Urine Anion Gap
A
Metabolic acidosis of extrarenal origin is usually suggested by the clinical circumstances but in uncertain cases is suggested by a large negative UAG
22
Q
Positive Urine Anion Gap
A
metabolic acidosis caused by distal (type 1) renal tubular acidosis, hypoaldosteronism (including type 4 renal tubular acidosis), and CKD.
23
Q
Delta-Delta
A
in anion gap acidosis, the expected ratio between the change in anion gap and the change in plasma [HCO3] concentration (Δ anion gap/Δ [HCO3]) is 1 to 2.
24
Q
If (Δ anion gap/Δ [HCO3]) is <1, consider
A
concurrent normal–anion gap acidosis
25
If (Δ anion gap/Δ [HCO3]) is >2 consider
concurrent metabolic alkalosis.
26
First step in assessing hyponatremia
is to classify it as either hyperosmolar or hypo-osmolar
27
Patients with hyponatremia and hyperosmolality have
pseudohyponatremia
In these patients, look for the presence of an osmotically active substance that is confined to the extracellular fluid
28
Conditions associated with pseudohyponatremia include:
hyperlipidemia, hyperproteinemia, and hyperglycemia
29
If the patient has hypo-osmolar hyponatremia, further classify the hyponatremia based on:
the patient's volume status.
30
Evaluating Hypo-osmolar Hyponatremia
Hypovolemia (hypotension, tachycardia)
Spot urine sodium 20:1
Urine osmolality >450 mosm/L
DDx: GI or kidney fluid losses, dehydration, adrenal insufficiency
31
Evaluating Hypo-osmolar Hyponatremia
Hypervolemia (edema, ascites)
Spot urine sodium 20:1
Urine osmolality >450 mosm/L
DDx: HF, cirrhosis, kidney failure
32
Evaluating Hypo-osmolar Hyponatremia
Euvolemia (normal volume)
Spot urine sodium >20 meq/L
BUN/creatinine 300 mosm/L
DDx SIADH, hypothyroidism
SIADH = syndrome of inappropriate antidiuretic hormone secretion.
33
Evaluating Hypo-osmolar Hyponatremia
Euvolemia (normal volume)
Spot urine sodium >20 meq/L
BUN/creatinine <20:1
Urine osmolality 50-100 mosm/L
Compulsive water drinking
34
Causes of SIADH include
malignancy (small cell lung cancer)
intracranial pathology
pulmonary diseases, especially those that increase intrathoracic pressure and decrease venous return to the heart
35
medications can cause SIADH, including
thiazides, SSRIs, tricyclic antidepressants, narcotics, phenothiazines, and carbamazepine (Tegretol).
36
DetectAlcohol Poisoning By Calculating the
Osmolal Gap = Measured - Calculated osmolality
Normal Osmolal gap is 10 mosm/kg H20; if large gap exists consider alcohol poisoning as the source of unmeasured osmols
37
Clues for Ingestion of Specific Types of Alcohol
Somnolence or coma and normal acid-base homeostasis
Isopropyl alcohol
38
Clues for Ingestion of Specific Types of Alcohol
Severe anion gap metabolic acidosis and acute visual symptoms or severe abdominal pain
Methanol (pancreatitis and retinal toxicity)
39
Clues for Ingestion of Specific Types of Alcohol
Severe anion gap metabolic acidosis and acute kidney injury
Ethylene glycol (metabolizes to glyoxylate and oxalic acid, which may cause calcium oxalate nephrolithiasis and acute kidney injury)
40
Clues for Ingestion of Specific Types of Alcohol
Anion gap metabolic acidosis and ketoacidosis
Ethanol
most common cause of alcohol poisoning
41
Cerebral salt wasting syndrome causes:
hypo-osmolar hyponatremia and laboratory parameters exactly like that of SIADH
Spot urine sodium >20 meq/L
BUN/creatinine 300 mosm/L
associated with hypovolemia, hypotension, and a neurosurgical procedure or subarachnoid hemorrhage within the previous 10 days.
42
Treatment for hyponatremia due to volume depletion, including hyponatremia from thiazide diuretics and cerebral salt wasting syndrome
normal saline
43
Treatment for hypo-osmolar hyponatremia associated with neurologic symptoms:
3% hypertonic saline infusion and furosemide to correct the serum sodium to 120 meq/L
44
Treatment for outpatients with SIADH:
Fluid restriction is used initially for asymptomatic outpatients with SIADH.
Demeclocycline can also be used for outpatients who do not respond to fluid restriction.
45
In hyponatremic patients, Do not correct the serum sodium faster than:
0.5 meq/h (about 12 meq over 24 hours).
46
Vaptan agents should not be used to treat:
hypovolemic hyponatremia
The IV V1 and V2 receptor antagonist conivaptan and the oral V2 receptor antagonist tolvaptan (vaptans) are approved for treatment of euvolemic and hypervolemic hyponatremia. Therapy must be initiated in the hospital and is very expensive. No data to date show the vaptans are associated with improved patient outcomes compared with conventional therapy.
47
Hypernatremia (causes)
serum sodium >145 meq/L
1. Defective thirst mechanism
2. inadequate access to water (older patients in nursing homes)
3. kidney concentrating defect (DI, most commonly due to lithium)
3. impaired pituitary secretion of ADH.
Most commonly, hypernatremia is due to loss of hypotonic fluids (GI, kidney, skin) with inadequate water replacement.
48
Most common causes of hyperkalemia include
1. hyporeninemic hypoaldosteronism
2. acute and chronic kidney failure
3. low urine flow states
4. medications (ACE inhibitors, ARBs, potassium-sparing diuretics, pentamidine, trimethoprim-sulfamethoxazole, and cyclosporine)
5. potassium shifts (rhabdomyolysis, hemolysis, hyperosmolality, insulin deficiency, β-adrenergic blockade, and metabolic acidosis)
Absolute levels of potassium cannot reliably determine if a life-threatening condition exists. Only ECG can assess the effect of hyperkalemia on the cardiac membrane.
49
Significant hyperkalemia associated with a normal ECG suggests:
pseudohyperkalemia
50
If hyperkalemia is associated with ECG changes or arrhythmias, begin:
IV calcium gluconate to stabilize the myocardium
shift potassium inside the cells with insulin and glucose or inhaled β-adrenergic agonists
removing potassium from the body with oral cation exchange resins, loop diuretics (particularly if volume is overloaded), and dietary potassium restriction
Hemodialysis is often needed to correct life-threatening hyperkalemia but is never the “first step” because of the time delay in initiating dialysis.
51
Most common causes of hypokalemia are:
Vomiting and diarrhea (urine [Cl–] <20 meq/L)
Use of diuretics (elevated urine [Cl–]).
52
Characteristic findings in severe hypophosphatemia are:
HF, muscle weakness, rhabdomyolysis, hemolytic anemia, and metabolic encephalopathy.
53
Common Causes of Hypophosphatemia:
1. refeeding after starvation
2. insulin administration for severe hyperglycemia
3. hungry bone syndrome following parathyroidectomy
4. respiratory alkalosis
5. chronic diarrhea
6. chronic alcoholism
7. hyperparathyroidism
8. vitamin D deficiency
54
Differential Diagnosis of Acute Kidney Injury - When you see this:
Minimal proteinuria, no hematuria or pyuria; presence of broad, muddy brown casts
Think of:
ATN
And Select:
FENa and/or spot urine sodium
55
Differential Diagnosis of Acute Kidney Injury - When you see this:
Erythrocytes, erythrocyte casts, or dysmorphic erythrocytes
Think of:
Glomerulonephritis
And Select as appropriate:
Titers for ANA, anti-dsDNA antibodies, and antistreptolysin O antibodies and C3, C4, and CH50; hepatitis and HIV serologies and cryoglobulins; p-ANCA/c-ANCA and anti-GBM antibodies
56
Differential Diagnosis of Acute Kidney Injury - When you see this:
Pyuria
Think of:
Pyelonephritis, AIN
And Select:
Culture urine
Examine medication list
57
Differential Diagnosis of Acute Kidney Injury - When you see this:
Livedo reticularis (violaceous reticular rash)
Think of:
Cholesterol emboli
And Select:
Look for previous vascular procedure (angiography)
Consider vasculitis
58
Differential Diagnosis of Acute Kidney Injury - When you see this:
Eosinophilia, eosinophiluria, and rash
Think of:
AIN, cholesterol emboli
And Select:
Examine medication list
Look for previous vascular procedure (angiography
59
Differential Diagnosis of Acute Kidney Injury - When you see this:
Hypercalcemia and anemia
Think of:
Multiple myeloma
And Select:
Serum and urine protein electrophoresis, quantitative immunoglobulins
60
Differential Diagnosis of Acute Kidney Injury - When you see this:
Nephrotic syndrome, urine protein >300 mg/dL
Think of:
Diabetes mellitus, renal vein thrombosis
And Select:
Plasma glucose
Renal vein Doppler study
61
Differential Diagnosis of Acute Kidney Injury - When you see this:
Obstruction on kidney ultrasound
Think of:
BPH, nephrolithiasis, obstructing malignant mass, retroperitoneal fibrosis
And Select:
Residual bladder volume, noncontrast CT or MRI
62
Differential Diagnosis of Acute Kidney Injury - When you see this:
Complete anuria
Think of:
Renal cortical necrosis
And Select:
Kidney ultrasonography
63
Differential Diagnosis of Acute Kidney Injury - When you see this:
Large kidneys on ultrasound
Think of:
Amyloidosis, diabetes (early), HIV nephropathy
And Select:
Serum protein electrophoresis, HIV serologic studies, plasma glucose
64
Differential Diagnosis of Acute Kidney Injury - When you see this:
Kidney failure following colonoscopy
Think of:
Phosphate-containing enemas (acute calcium phosphate crystal deposition in the kidneys)
And Select:
Supportive care (fluids, stop ACE inhibitors, ARBs, NSAIDs)
65
Differential Diagnosis of Acute Kidney Injury - When you see this:
Recent abdominal surgery, hemorrhage or acute pancreatitis
Think of:
Abdominal compartment syndrome
And Select:
Intravesicular pressure >20 mm Hg
66
Differential Diagnosis of Acute Kidney Injury - When you see this:
Peripheral blood smear schistocytes, thrombocytopenia
Think of:
Thrombotic microangiopathy (HUS/TTP, DIC, scleroderma renal crisis)
And Select:
As indicated, CBC, coagulation parameters
67
Differential Diagnosis of Acute Kidney Injury - When you see this:
Urine dipstick positive for blood, no erythrocytes on urinalysis
Think of:
Hemolysis, rhabdomyolysis
And Select:
Serum CK, serum haptoglobin, reticulocyte count, peripheral blood smear
68
Differential Diagnosis of Acute Kidney Injury - When you see this:
AKI associated with acute leukemia or lymphoma or its treatment
Think of:
Tumor lysis syndrome
And Select:
Uric acid, phosphorus, potassium (all elevated)
69
Acute Kidney Injury (AKI) is divided into two categories:
oliguric (≤400 mL/24 h) and nonoliguric (>400 mL/24 h) forms.
70
FENa is used to help differentiate:
prerenal azotemia from ATN
FENa = ([Urine Na]/[Serum Na] × 100%)
71
FENa =
FENa = ([Urine Na]/[Serum Na] × 100%)
72
Interpretation of the FENa in patients with oliguria:
If >1%, consider:
ATN or AIN.
Urinalysis will help define the underlying pathology (AIN is associated with leukocytes and leukocyte casts, occasionally with eosinophils).
73
Interpretation of the FENa in patients with oliguria:
If <10 meq/L) and urinalysis is benign, consider
prerenal azotemia
74
Interpretation of the FENa in patients with oliguria:
If <10 meq/L) and urinalysis shows erythrocytes, dysmorphic erythrocytes, and erythrocyte casts or proteinuria, consider
glomerulonephritis
75
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hypertension
Select:
An ACE inhibitor or ARB; use a loop diuretic rather than a thiazide for GFR <30 mL/min/1.73m2
Examples loop diuretics
Furosemide
Bumetanide
76
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Serum protein-creatinine ratio ≥200 mg/mg
Select:
Titrate ACE inhibitor and ARB to achieve minimal proteinuria even if patient is normotensive
77
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hemoglobin A1c >7%
Select:
More intensive intervention to maintain hemoglobin A1c <7%
78
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Anemia
Select:
Erythropoietin to maintain hemoglobin levels of 10-11 g/dL and iron to maintain iron stores (always check iron levels before starting erythropoietin)
79
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hypocalcemia, hyperphosphatemia
Select:
Phosphate binders (calcium acetate, calcium carbonate, sevelamer) to maintain [PO4] between 3.5-5.5 mg/dL
cinacalcet, a calcimimetic, is approved for treatment of secondary hyperparathyroidism in dialysis patients
80
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Metabolic acidosis
Select:
Alkali therapy to maintain [HCO3] between 20-26 meq/L
81
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Lipids
Select:
Statin therapy to reduce LDL cholesterol <100 mg/dL
82
Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Vitamin D deficiency
Select:
Calcitriol (or vitamin D analogues)
83
Loop diuretics
Furosemide
| Bumetanide (much more potent)
84
DDx Chronic Kidney Disease
```
Diabetes
Glomerular disease
Tubulointerstitial disease
Vascular disease
Structural disease
```
85
Features and chronic kidney disease caused by:
Diabetic kidney disease
Look for early microalbuminuria (spot albumin-creatinine ratio, 30-300 mg/g), followed by overt proteinuria, declining GFR, and a bland urine sediment. The presence of retinopathy strongly suggests coexisting diabetic nephropathy.
86
Features and chronic kidney disease caused by:
Glomerular disease
lomerular hematuria, proteinuria, and hypertension, often with other systemic manifestations (lupus nephritis and postinfectious glomerulonephritis)
If nephrotic syndrome is present, look for focal segmental glomerulosclerosis, membranous nephropathy, minimal change disease, and amyloidosis.
kidney biopsy is often needed to make a specific diagnosis and guide therapy.
87
Features and chronic kidney disease caused by:
Tubulointerstitial disease
Look for proteinuria, glycosuria, concentrating defect, sterile pyuria, and leukocyte casts, as well as papillary necrosis on ultrasound
Consider analgesic nephropathy (medication use, papillary necrosis), infection (TB, legionnaires disease, leptospirosis), allergic drug reaction (eosinophilia, eosinophiluria), autoimmune disorder (SLE, sarcoidosis, Sjögren syndrome), and lead nephropathy (occupational exposure).
88
Features and chronic kidney disease caused by:
Vascular disease
Look for hematuria, proteinuria, and associated systemic illness.
Vasculitis often presents with rapidly progressive glomerulonephritis and palpable purpura (leukocytoclastic vasculitis).
89
Features and chronic kidney disease seen after kidney transplantation:
chronic allograft nephropathy, drug toxicity (cyclosporine), polyomavirus BK infection, or recurrence of disease
90
Features and chronic kidney disease caused by:
Structural disease (polycystic kidney disease)
Look for hypertension, hematuria, palpable kidneys (advanced disease), family history of CKD.
91
Nephrotic Syndrome
Proteinuria (>3.5 g/24 h), hypoalbuminemia, and edema
Other findings may include hyperlipidemia with lipiduria (“Maltese cross” fat droplets in urine seen with polarized light microscopy)
Massive proteinuria results in loss of anticoagulant proteins C and S and places the patient at risk for venous thromboembolism.
92
Causes of Acute Glomerulonephritis
Acute poststreptococcal glomerulonephritis
IgA nephropathy
Idiopathic membranoproliferative glomerulonephritis (MPGN)
Secondary MPGN
ANCA-associated glomerulonephritis (prototype is granulomatosis with polyangiitis [Wegener granulomatosis])
Anti-GBM antibody disease (Goodpasture disease)
Cryoglobulinemia
93
Clinical Features of:
Acute poststreptococcal glomerulonephritis
**** Hematuria occurs 1-3 weeks after sore throat. ****
Serum complement levels are low, and anti-DNAse B assay is positive.
Kidney biopsy shows crescents, subepithelial deposits (humps), and mesangial deposits on electron microscopy.
94
Clinical Features of:
IgA nephropathy
*** Hematuria occurs 1-2 days after a sore throat. ****
Clinical manifestations range from asymptomatic microscopic hematuria to acute or chronic kidney failure.
IgA deposits are present on the immunofluorescence staining of the kidney biopsy.
95
Clinical Features of:
Idiopathic membranoproliferative glomerulonephritis (MPGN)
Hypocomplementemia, thickened capillary loops on light microscopy, and immune deposits are seen on electron microscopy.
96
Clinical Features of:
Secondary membranoproliferative glomerulonephritis (MPGN)
MPGN is seen in the setting of a chronic infection (HCV, syphilis, endocarditis, HIV), systemic disease (diabetes mellitus, RA), drugs (NSAIDs, penicillamine), and solid tumors (breast, colon, lung, kidney).
97
Clinical Features of:
ANCA-associated glomerulonephritis (prototype is granulomatosis with polyangiitis [Wegener granulomatosis])
Nasal congestion, ulceration, chronic sinusitis, and/or pulmonary (often nodular) infiltrates are found.
Pathologic findings include a proliferative glomerulonephritis in the setting of positive c-ANCA or p-ANCA.
98
Clinical Features of:
Anti-GBM antibody disease (Goodpasture disease)
Glomerulonephritis and pulmonary hemorrhage are present.
| Linear staining of the GBM seen on immunofluorescence microscopy.
99
Clinical Features of:
Cryoglobulinemia
Palpable purpura, arthritis, neuropathy, and digital ischemia are present.
Low complement levels and cryoglobulins are present in the serum or on kidney biopsy specimens.
Can be associated with HCV.
100
If you see this…
Pulmonary infiltrates or nodules, sinusitis, nasal ulcers, saddle nose deformity, or glomerulonephritis
Think this…
Granulomatosis with polyangiitis (Wegener granulomatosis)
**** Nearly 95% of patients with granulomatosis with polyangiitis have sinus disease. The absence of sinus disease rules out this disorder.****
Choose this ...
c-ANCA, p-ANCA, and antiproteinase-3 (anti-PR3)
101
If you see this…
Glomerulonephritis and alveolar hemorrhage
Think this…
Anti-GBM antibody disease (Goodpasture disease)
Choose this ...
Anti-GBM antibodies; immunofluorescence microscopy revealing linear staining of IgG lining the GBM
102
If you see this…
Pulmonary hemorrhage, nephritis, arthralgia, serositis, rash, anemia, thrombocytopenia, leukopenia
Think this…
SLE
Choose this ...
Anti-dsDNA or anti-Sm antibodies
103
If you see this…
Bacterial endocarditis or cryoglobulinemia
Think this…
Immune complex-mediated disorders
Choose this ...
Serum cryoglobulins and blood cultures
104
Important risk factors for kidney stone formation include:
1. insufficient fluid intake
2. increased dietary sodium and protein intake
3. hypercalciuria, hyperuricemia, hyperoxaluria
4. low urine citrate levels (citrate inhibits crystal formation)
5. primary hyperparathyroidism with hypercalciuria
6. metabolic syndrome and type 2 diabetes mellitus
7. recurrent UTIs with urease-splitting organisms such as Klebsiella and Proteus (struvite stones)
